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http://purl.uniprot.org/citations/22221582http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22221582http://www.w3.org/2000/01/rdf-schema#comment"We hypothesized that oxidative stress may contribute to the development of hypertrophy observed in mice with cardiac specific ablation of the insulin sensitive glucose transporter 4 gene (GLUT4, G4H(-/-) ). Measurements of oxidized glutathione (GSSG) in isolated mitochondria and whole heart homogenates were increased resulting in a lower ratio of reduced glutathione (GSH) to GSSG. Membrane translocation of the p67(phox) subunit of cardiac NADPH oxidase 2 (NOX2) was markedly increased in G4H(-/-) mice, suggesting elevated activity. To determine if oxidative stress was contributing to cardiac hypertrophy, 4-week-old control (Con) and G4H(-/-) mice were treated with either tempol (T, 1 mm, drinking water), a whole cell antioxidant, or Mn(III) tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP, 10 mg·kg(-1) , intraperitoneally), a mitochondrial targeted antioxidant, for 28 days. Tempol attenuated cardiac hypertrophy in G4H(-/-) mice (heart : tibia, Con 6.82 ± 0.35, G4H(-/-) 8.83 ± 0.34, Con + T 6.82 ± 0.46, G4H(-/-) + T 7.57 ± 0.3), without changing GSH : GSSG, glutathione peroxidase 4 or membrane translocation of the p67(phox) . Tempol did not modify phosphorylation of glycogen synthase kinase 3β or thioredoxin-2. In contrast, MnTBAP lowered mitochondrial GSSG and improved GSH : GSSG, but did not prevent hypertrophy, indicating that mitochondrial oxidative stress may not be critical for hypertrophy in this model. The ability of tempol to attenuate cardiac hypertrophy suggests that a cytosolic source of reactive oxygen species, probably NOX2, may contribute to the hypertrophic phenotype in G4H(-/-) mice."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.org/dc/terms/identifier"doi:10.1111/j.1742-4658.2011.08450.x"xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Huang Y."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Jin H."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Hu E."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Boudina S."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Abel E.D."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Jalili T."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Wende A.R."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/author"Nunthakungwan O."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/name"FEBS J"xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/pages"599-611"xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/title"Cytosolic, but not mitochondrial, oxidative stress is a likely contributor to cardiac hypertrophy resulting from cardiac specific GLUT4 deletion in mice."xsd:string
http://purl.uniprot.org/citations/22221582http://purl.uniprot.org/core/volume"279"xsd:string
http://purl.uniprot.org/citations/22221582http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22221582
http://purl.uniprot.org/citations/22221582http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22221582
http://purl.uniprot.org/uniprot/#_A0A0G2JDD0-mappedCitation-22221582http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22221582
http://purl.uniprot.org/uniprot/#_A0A087WPH0-mappedCitation-22221582http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22221582
http://purl.uniprot.org/uniprot/#_P14142-mappedCitation-22221582http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22221582
http://purl.uniprot.org/uniprot/#_J3QK17-mappedCitation-22221582http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22221582
http://purl.uniprot.org/uniprot/#_J3QMU2-mappedCitation-22221582http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22221582
http://purl.uniprot.org/uniprot/#_J3QMX9-mappedCitation-22221582http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22221582